Methyl cinnamate, an active component of Zanthoxylum armatum , is a widely used natural flavor compound with antimicrobial and tyrosinase inhibitor activities. However, the underlying bioactivity and molecular mechanisms of methyl cinnamate on adipocyte function and metabolism remain unclear. The aim of this study was to investigate the inhibitory effect of methyl cinnamate on adipogenesis in 3T3-L1 preadipocytes. Methyl cinnamate markedly suppressed triglyceride accumulation associated with down-regulation of adipogenic transcription factor expression, including sterol regulatory element binding protein-1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), and CCAAT/enhancer-binding protein α (C/EBPα). Additionally, methyl cinnamate-inhibited PPARγ activity and adipocyte differentiation were partially reversed by the PPARγ agonist troglitazone. Furthermore, methyl cinnamate stimulated Ca(2+)/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and phospho-AMP-activated protein kinase (AMPK) expression during adipogenesis. This study first revealed methyl cinnamate has antiadipogenic activity through mechanisms mediated, in part, by the CaMKK2-AMPK signaling pathway in 3T3-L1 cells.

This study examined the anti-herpes simplex virus type I activity of the major constituents of several essential oils. Plaque reduction assays were performed to evaluate anti-herpes simplex virus type I activity. Thymol and carvacrol both possessed significant antiviral activity with an IC₅₀ of 7  µM, and herpes simplex virus type I was 90 % inactivated within 1 hr. The mode of antiviral action was shown to affect the virion directly. Evidence was also observed by electron microscopy. Evaluation of the structural requirements for antiviral activity of thymol-related monoterpenoids revealed that aliphatic side chains had a minor effect, while a hydrophilic group on the benzene ring was sufficient for activity. Our results suggest that thymol and carvacrol are potential candidates for topical therapeutic application to reduce herpes simplex virus transmission.